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Relative mass index of the mice brain and liver (g of organ mass/g of body weight) of control group mice and mice orally treated with a Na 2 SeO 3 solution for 8 weeks. The model of selenium exposure to mice is described in the Methods section. The data were obtained by measuring the body weight and organ mass of 16 mice in each group. Results were expressed as the mean ± SEM. *-differences are statistically significant in comparison to the control group; p < 0.05.
Source publication
Selenium is an essential trace element that maintains normal brain function, mainly due its antioxidant properties. Although the amount of Se in the body is tightly regulated by the liver, both an excess of and deficiency in Se can modulate the cellular redox status and affect the homeostasis of other essential elements for both humans and animals....
Contexts in source publication
Context 1
... the relative mass index of mouse brain and liver was evaluated after 8 weeks of exposure to Na 2 SeO 3 . The data in Figure 2 demonstrate that both the 0.2 and 0.4 mg/kg BW of Se doses have reduced the liver mass index; however, they had no significant effect on the mass index of the brain. Mice treated with the 0.2 and 0.4 mg/kg BW of Se doses demonstrated a statistically significant reduction in the relative liver mass index by 20.8% and 18.2%, respectively, as compared to the control. ...
Context 2
... the relative mass index of mouse brain and liver was evaluated after 8 weeks of exposure to Na2SeO3. The data in Figure 2 demonstrate that both the 0.2 and 0.4 mg/kg BW of Se doses have reduced the liver mass index; however, they had no significant effect on the mass index of the brain. Mice treated with the 0.2 and 0.4 mg/kg BW of Se doses demonstrated a statistically significant reduction in the relative liver mass index by 20.8% and 18.2%, respectively, as compared to the control. ...
Context 3
... the end of experimental period, a tendency of an increase (11-14%) in the relative brain mass index of Se-treated mice was observed; however, this change was not statistically significant. Figure 2. Relative mass index of the mice brain and liver (g of organ mass/g of body weight) of control group mice and mice orally treated with a Na2SeO3 solution for 8 weeks. ...
Context 4
... the next step of our study, we sought to assess whether the Se-induced lipid peroxidation, observed in our study, was somehow related to the activity of an antioxidant system enzyme catalase, which does not depend on Se as a cofactor. Scientific evidence suggests that excess Se increases both the amount of lipid peroxides as well as the amount of hydrogen peroxide (H 2 O 2 ), which is a substrate for catalase [48]. Catalase then breaks down H 2 O 2 molecules into oxygen and water, thus preventing them from accumulating in cells and causing oxidative damage [24]. ...
Citations
... In the biological process, Se participates in the redox mechanism in the form of selenocysteine and is incorporated into the active site of selenoproteins such as glutathione peroxidases (GPX) and thioredoxin reductases (TXNRD). GPX is acknowledged as the primary enzyme that counteracts ROS and reduces neuronal damage from oxidative stress [50]. Though biological evidence explaining the reversed association of cognitive performance with high levels of Se is scarce, previous studies have proposed the threshold range of protective Se and the possible toxicity of Se [51,52]. ...
Many studies suggest a significant association between individual essential trace elements (ETEs) and cognitive impairment in older adults, but evidence of the synchronized effect of multiple ETEs on cognitive function is lacking. We investigated the association between multiple ETEs, cognitive impairment with no dementia (CIND), and executive function in older Korean adults, using the Bayesian kernel machine regression (BKMR) model. Three hundred and thirty-six older adults were included as the study population and classified as the CIND and control groups. Blood manganese (Mn), copper (Cu), zinc (Zn), selenium (Se), and molybdenum (Mo) were measured as relevant ETEs. The frontal/executive tests included digit symbol coding (DSC), the Korean color word Stroop test (K-CWST), a controlled oral word association test (COWAT), and a trial-making test (TMT). Overall, the BKMR showed a negative association between multiple ETEs and the odds of CIND. Mn was designated as the most dominant element associated with the CIND (PIP = 0.6184), with a U-shaped relationship. Cu and Se levels were positively associated with the K-CWST percentiles (β = 31.78; 95% CI: 13.51, 50.06) and DSC percentiles (β = 25.10; 95% CI: 7.66, 42.53), respectively. Our results suggest that exposure to multiple ETEs may be linked to a protective mechanism against cognitive impairment in older adults.
... Each sample underwent nitration using 25% nitric acid, dilution with 30% hydro-gen peroxide, and was ultimately stabilized in ultra-pure water. An inductively coupled plasma mass spectrometry (ICP-MS) parameter iCAPQ instrument (Thermo Fisher Scientific, Waltham, MA, USA) was used to conduct the elemental analysis (Staneviciene et al., 2022). We maintained result accuracy by implementing internal and external quality controls, which included utilizing ultra-pure water and reagents. ...
Non‐invasive transcranial direct‐current stimulation (tDCS) is a safe ischaemic stroke therapy. Cathodal bilateral tDCS (BtDCS) is a modified tDCS approach established by us recently. Because selenium (Se) plays a crucial role in cerebral ischaemic injury, we investigated whether cathodal BtDCS conferred neuroprotection via regulating Se‐dependent signalling in rat cerebral ischaemia–reperfusion (I/R) injury. We first showed that the levels of Se and its transport protein selenoprotein P (SEPP1) were reduced in the rat cortical penumbra following I/R, whereas cathodal BtDCS prevented the reduction of Se and SEPP1. Interestingly, direct‐current stimulation (DCS) increased SEPP1 level in cultured astrocytes subjected to oxygen‐glucose deprivation reoxygenation (OGD/R) but had no effect on SEPP1 level in OGD/R‐insulted neurons, indicating that DCS may increase Se in ischaemic neurons by enhancing the synthesis and secretion of SEPP1 in astrocytes. We then revealed that DCS reduced the number of injured mitochondria in OGD/R‐insulted neurons cocultured with astrocytes. DCS and BtDCS prevented the reduction of the mitochondrial quality‐control signalling, vesicle‐associated membrane protein 2 (VAMP2) and syntaxin‐4 (STX4), in OGD/R‐insulted neurons cocultured with astrocytes and the ischaemic brain respectively. Under the same experimental conditions, downregulation of SEPP1 blocked DCS‐ and BtDCS‐induced upregulation of VAMP2 and STX4. Finally, we demonstrated that cathodal BtDCS increased Se to reduce infract volume following I/R. Together, the present study uncovered a molecular mechanism by which cathodal BtDCS confers neuroprotection through increasing SEPP1 in astrocytes and subsequent upregulation of SEPP1/VAMP2/STX4 signalling in ischaemic neurons after rat cerebral I/R injury. image
Key points
Cathodal bilateral transcranial direct‐current stimulation (BtDCS) prevents the reduction of selenium (Se) and selenoprotein P in the ischaemic penumbra.
Se plays a crucial role in cerebral ischaemia injury.
Direct‐current stimulation reduces mitochondria injury and blocks the reduction of vesicle‐associated membrane protein 2 (VAMP2) and syntaxin‐4 (STX4) in oxygen‐glucose deprivation reoxygenation‐insulted neurons following coculturing with astrocytes.
Cathodal BtDCS regulates Se/VAMP2/STX4 signalling to confer neuroprotection after ischaemia.
... Irrespective, Fe and Cu are known to play essential regulatory roles in neuronal development by regulating the redox system, acting as essential metal cofactors in the DNA base excision repair pathway, and contributing to neurotransmitter synthesis (Wandt, 2021). Further, the cellular pathways of Mg and Ca homeostasis are also known to interact and regulate cell growth, differentiation, and death (Staneviciene, 2022). While these elements serve essential roles in neuronal development and function (Wandt, 2021;Staneviciene, 2022), imbalances in their concentrations may lead to deleterious neuronal impacts that manifest as behavioural and neurobiological alterations in MIA exposed offspring. ...
... Further, the cellular pathways of Mg and Ca homeostasis are also known to interact and regulate cell growth, differentiation, and death (Staneviciene, 2022). While these elements serve essential roles in neuronal development and function (Wandt, 2021;Staneviciene, 2022), imbalances in their concentrations may lead to deleterious neuronal impacts that manifest as behavioural and neurobiological alterations in MIA exposed offspring. Therefore, appropriate regulation of elemental homeostasis within the foetal brain is fundamental for neuronal development. ...
... Our results are consistent with the data provided by other scientists, which confirm Se accumulation in the liver, as well as an increased Se concentration in the blood of various species [61,[64][65][66]. A comparison of our results with the results of our previously published study, when mice were exposed to the same (0.4 mg Se/kg BW) dose of inorganic Se (Na selenite), showed that blood Se levels in mice exposed to SeMet were three times higher compared with its level in sodium selenite-exposed mouse blood [67]. According to our results, the amount of Se accumulated in the liver of control mice reached 0.615 ± 0.095 µg/g tissue; other authors indicate slightly lower, however, comparable amounts of Se (0.44 ± 0.26 µg/g) in the liver of control mice [68]. ...
... According to our results, the amount of Se accumulated in the liver of control mice reached 0.615 ± 0.095 µg/g tissue; other authors indicate slightly lower, however, comparable amounts of Se (0.44 ± 0.26 µg/g) in the liver of control mice [68]. Eight-week-long mouse exposure to 0.4 mg of SeMet increased the concentration of accumulated Se in the liver up to 9.49 ± 0.33 µg/g, while results of our previous study showed that the concentration of Se accumulated in the liver of mice exposed to the same dose of sodium selenite was 2.11 ± 0.045 µg/g [67], i.e., 4.5 times lower. Determination of Se contents in the brains of mice revealed that the brain accumulates 10 times less Se than the liver; however, the long-term administration of SeMet solution increased brain Se more than 42 times (2.57 ...
... ± 0.147 µg/g) compared to that in the control. Meanwhile, after mouse exposure to 0.4 mg of sodium selenite for the same period, the concentration of Se accumulated in the brain was only 2.5 times higher as compared to that in the control [67]. Therefore, a summarization of our results shows that the absorption of organic Se is significantly more efficient than inorganic Se. ...
(1) In this study we determined the effect of long-term selenomethionine administration on the oxidative stress level and changes in antioxidant protein/enzyme activity; mRNA expression; and the levels of iron, zinc, and copper. (2) Experiments were performed on 4–6-week-old BALB/c mice, which were given selenomethionine (0.4 mg Se/kg b.w.) solution for 8 weeks. The element concentration was determined via inductively coupled plasma mass spectrometry. mRNA expression of SelenoP, Cat, and Sod1 was quantified using real-time quantitative reverse transcription. Malondialdehyde content and catalase activity were determined spectrophotometrically. (3) After long-term SeMet administration, the amount of Se increased by 12-fold in mouse blood, 15-fold in the liver, and 42-fold in the brain, as compared to that in the control. Exposure to SeMet decreased amounts of Fe and Cu in blood, but increased Fe and Zn levels in the liver and increased the levels of all examined elements in the brain. Se increased malondialdehyde content in the blood and brain but decreased it in liver. SeMet administration increased the mRNA expression of selenoprotein P, dismutase, and catalase, but decreased catalase activity in brain and liver. (4) Eight-week-long selenomethionine consumption elevated Se levels in the blood, liver, and especially in the brain and disturbed the homeostasis of Fe, Zn, and Cu. Moreover, Se induced lipid peroxidation in the blood and brain, but not in the liver. In response to SeMet exposure, significant up-regulation of the mRNA expression of catalase, superoxide dismutase 1, and selenoprotein P in the brain, and especially in the liver, was determined.
The objective of this study is to gain insights into the underlying metabolic transformations that occurred during the whole progression of cecal ligation and puncture (CLP)-induced sepsis, thus providing new targets for its treatment. High-performance liquid chromatography of quadrupole time of flight mass spectrometry (HPLC-Q-TOF-MS/MS) combined with multivariate statistical techniques was used to detect the s in serum from septic mice. Fifty male mice were divided into two groups, including the sham group (n = 7) and the CLP-induced sepsis group (n = 43). Animals were sacrificed at 1, 3, 5, and 7 days post-CLP and then serum were collected for metabolomic analysis. Multivariate regression analysis was carried out through MetaboAnalyst 5.0, including principal component analysis (PCA) and partial least squares discriminant analysis (PLS-DA), to identify the s and screen out the related differential metabolites. Besides, the KEGG pathway analysis was used to analyze the related metabolic pathways in which the identified metabolites were involved. Based on the fold change (FC > 2.0 or <0.5), variable important in projection (VIP > 1.2), and P value (P < 0.05), we found 26, 17, 21, and 17 metabolites in septic mice at 1, 3, 5, and 7 days post-CLP, respectively, compared with that of the sham group. The PCA and PLS-DA pattern recognition showed a cluster-type distribution between the sham group and the CLP group. Dysregulated amino acid metabolism, as well as disturbed nucleotide metabolism, is observed. Several important metabolic pathways were identified between the sham group and the CLP group. Among them, phenylalanine metabolism, phenylalanine, tyrosine, and tryptophan biosynthesis showed striking at day 1 post-CLP. At day 3, phenylalanine, tyrosine, and tryptophan biosynthesis changed significantly. However, as the disease process, only pyrimidine metabolism showed the most significant alternation, compared to the sham group. Several differential metabolites were identified in the CLP group compared with that of the sham group and they were presented with dynamic alternation at different time points post-CLP, indicating metabolic disturbance occurred throughout the whole sepsis progression.
Ferropenic anemy is the leading iron deficiency disease in the world. The aim was to encapsulate erythrocytes extracted from the blood of Cavia porcellus, in matrices of tara gum and native potato starch. For microencapsulation, solutions were prepared with 20% erythrocytes; and encapsulants at 5, 10, and 20%. The mixtures were spray-dried at 120 and 140 °C. The iron content in the erythrocytes was 3.30 mg/g and between 2.32 and 2.05 mg/g for the encapsulates (p < 0.05). The yield of the treatments varied between 47.84 and 58.73%. The moisture, water activity, and bulk density were influenced by the temperature and proportion of encapsulants. The total organic carbon in the atomized samples was around 14%. The particles had diverse reddish tonalities, which were heterogeneous in their form and size; openings on their surface were also observed by SEM. The particle size was at the nanometer level, and the zeta potential (ζ) indicated a tendency to agglomerate and precipitation the solutions. The presence of iron was observed on the surface of the atomized by SEM-EDX, and FTIR confirmed the encapsulation due to the presence of the chemical groups OH, C-O, C-H, and N-H in the atomized. On the other hand, high percentages of iron release in vitro were obtained between 88.45 and 94.71%. The treatment with the lowest proportion of encapsulants performed at 140 °C obtained the best results and could potentially be used to fortify different functional foods.
